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Category: genetics

Scientists Turned Our Cells Into Quantum Computers—Sort Of

For the protein qubit to “encode” more information about what is going on inside a cell, the fluorescent protein needs to be genetically engineered to match the protein scientists want to observe in a given cell. The glowing protein is then attached to the target protein and zapped with a laser so it reaches a state of superposition, turning it into a nano-probe that picks up what is happening in the cell. From there, scientists can infer how a certain biological process happens, what the beginnings of a genetic disease look like, or how cells respond to certain treatments.

And eventually, this kind of sensing could be used in non-biological applications as well.

“Directed evolution on our EYFP qubit could be used to optimize its optical and spin properties and even reveal unexpected insights into qubit physics,” the researchers said. “Protein-based qubits are positioned to take advantage of techniques from both quantum information sciences and bioengineering, with potentially transformative possibilities in both fields.”

Study finds cell memory can be more like a dimmer dial than an on/off switch

When cells are healthy, we don’t expect them to suddenly change cell types. A skin cell on your hand won’t naturally morph into a brain cell, and vice versa. That’s thanks to epigenetic memory, which enables the expression of various genes to “lock in” throughout a cell’s lifetime. Failure of this memory can lead to diseases, such as cancer.

Traditionally, scientists have thought that epigenetic memory locks genes either “on” or “off” — either fully activated or fully repressed, like a permanent Lite-Brite pattern. But MIT engineers have found that the picture has many more shades.

In a new study appearing today in Cell Genomics, the team reports that a cell’s memory is set not by on/off switching but through a more graded, dimmer-like dial of gene expression.

CRISPR’s efficiency triples with DNA-wrapped nanoparticles

EVANSTON, IL. — With the power to rewrite the genetic code underlying countless diseases, CRISPR holds immense promise to revolutionize medicine. But until scientists can deliver its gene-editing machinery safely and efficiently into relevant cells and tissues, that promise will remain out of reach.

Now, Northwestern University chemists have unveiled a new type of nanostructure that dramatically improves CRISPR delivery and potentially extends its scope of utility.

Called lipid nanoparticle spherical nucleic acids (LNP-SNAs), these tiny structures carry the full set of CRISPR editing tools — Cas9 enzymes, guide RNA and a DNA repair template — wrapped in a dense, protective shell of DNA. Not only does this DNA coating shield its cargo, but it also dictates which organs and tissues the LNP-SNAs travel to and makes it easier for them to enter cells.

New system delivers CRISPR machinery more safely and effectively into cells.

Satiation variability prediction using AI for obesity treatment

Meal size and termination is regulated by a process called satiation, which varies widely among adults with obesity.

The researchers assessed calories to satiation (CTS) and integrated a machine learning genetic risk score (CTSGRS) to predict obesity treatment outcomes.

High CTS or CTSGRS identified individuals who responded better to phentermine-topiramate, whereas low CTS or CTSGRS predicted greater weight loss with liraglutide, highlighting personalized obesity therapy.

Heterochronic myeloid cell replacement reveals the local brain environment as key driver of microglia aging

Aging, the key risk factor for cognitive decline, impacts the brain in a region-specific manner, with microglia among the most affected cell types. However, it remains unclear whether this is intrinsically mediated or driven by age-related changes in neighboring cells. Here, we describe a scalable, genetically modifiable system for in vivo heterochronic myeloid cell replacement. We find reconstituted myeloid cells adopt region-specific transcriptional, morphological and tiling profiles characteristic of resident microglia. Young donor cells in aged brains rapidly acquired aging phenotypes, particularly in the cerebellum, while old cells in young brains adopted youthful profiles. We identified STAT1-mediated signaling as one axis controlling microglia aging, as STAT1-loss prevented aging trajectories in reconstituted cells. Spatial transcriptomics combined with cell ablation models identified rare natural killer cells as necessary drivers of interferon signaling in aged microglia. These findings establish the local environment, rather than cell-autonomous programming, as a primary driver of microglia aging phenotypes.

Claire Gizowski, Galina Popova, Heather Shin, Wendy Craft, Wenjun Kong, Bernd J Wranik, Yuheng C Fu, Tzuhua D Lin, Baby Martin-McNulty, Po-Han Tai, Kayla Leung, Nicole Fong, Devyani Jogran, Agnieszka Wendorff, David Hendrickson, Astrid Gillich, Andy Chang, Oliver Hahn are current or former employees of Calico Life Sciences LLC. The remaining authors declare no competing interest.

Diet, Supplements Of A Longevity Scientist (Blood Test #5 In 2025)

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Researchers uncover critical genetic drivers of the gut’s ‘nervous system’ development

Vanderbilt researchers, including those from the Vanderbilt Brain Institute, have made significant strides in understanding how the enteric nervous system—sometimes called the “brain” of the gut—forms and functions.

In a study published in Cellular and Molecular Gastroenterology and Hepatology, the lab of principal investigator, Michelle Southard-Smith, sheds light on how the SOX10 protein contributes to the development of gut cells that play a role in gastrointestinal motility, or how food moves through the digestive system.

The paper is titled “Single Cell Profiling in the Sox10Dom Hirschsprung Mouse Implicates Hox genes in Enteric Neuron Trajectory Allocation.”

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